The search for an antiviral lead molecule to combat the neglected emerging Oropouche virus
•Oropouche virus (OROV) is the causative agent of a dengue-like febrile illness transmitted by mosquitoes with epidemic potential.•Wedelolactone (WDL) is a putative natural antiviral compound known to inhibit viral proteins and replication processes.•Our study demonstrated in silico and in vitro ant...
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Published in: | Current research in microbial sciences Vol. 6; p. 100238 |
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Main Authors: | , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier B.V
01-01-2024
Elsevier |
Subjects: | |
Online Access: | Get full text |
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Summary: | •Oropouche virus (OROV) is the causative agent of a dengue-like febrile illness transmitted by mosquitoes with epidemic potential.•Wedelolactone (WDL) is a putative natural antiviral compound known to inhibit viral proteins and replication processes.•Our study demonstrated in silico and in vitro anti-OROV effects by WDL associated with the viral endonuclease interaction and inhibition.
Oropouche virus (OROV) is a member of the Peribunyaviridae family and the causative agent of a dengue-like febrile illness transmitted by mosquitoes. Although mild symptoms generally occur, complications such as encephalitis and meningitis may develop. A lack of proper diagnosis, makes it a potential candidate for new epidemics and outbreaks like other known arboviruses such as Dengue, Yellow Fever and Zika virus. The study of natural molecules as potential antiviral compounds is a promising alternative for antiviral therapies. Wedelolactone (WDL) has been demonstrated to inhibit some viral proteins and virus replication, making it useful to target a wide range of viruses. In this study, we report the in silico effects of WDL on the OROV N-terminal polymerase and its potential inhibitory effects on several steps of viral infection in mammalian cells in vitro, which revealed that WDL indeed acts as a potential inhibitor molecule against OROV infection.
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 2666-5174 2666-5174 |
DOI: | 10.1016/j.crmicr.2024.100238 |